3035-73-2

Usage

Uses

Used in Pharmaceutical Research:
6-chloro-9-methyl-9H-purin-2-amine is used as a building block for the development of purine-containing compounds, specifically for the creation of antiviral and anticancer drugs. Its unique structure and bioactivity make it a valuable asset in the design and synthesis of novel therapeutic agents.
Used in the Synthesis of Nucleotide Analogues:
In the field of organic chemistry, 6-chloro-9-methyl-9H-purin-2-amine is utilized as an intermediate in the synthesis of nucleotide analogues. These analogues are essential in various biological and medicinal applications, including the development of antiviral agents that target specific viral replication mechanisms.
Used in the Study of Purine Metabolism:
6-chloro-9-methyl-9H-purin-2-amine contributes to the understanding of purine metabolism, a critical process in the biosynthesis and degradation of purines, which are essential components of DNA and RNA. Research involving 6-chloro-9-methyl-9H-purin-2-amine aids in uncovering the mechanisms of purine-related diseases and the development of targeted therapies.
Used in the Study of Signal Transduction Pathways:
6-chloro-9-methyl-9H-purin-2-amine is also employed in the investigation of signal transduction pathways within the human body. Given its role in the purine base structure, 6-chloro-9-methyl-9H-purin-2-amine provides insights into how signals are transmitted within cells, which is vital for the regulation of cellular processes and the development of new drugs targeting these pathways.

Upstream product

• 10310-21-1 2-Amino-6-chloropurin 
• 74-88-4 methyl iodide 
• 122-51-0 orthoformic acid triethyl ester 
• 330433-43-7 6-chloro-N⁴-methyl-pyrimidine-2,4,5-triamine 
• 327161-48-8 N₁-(6-chloro-9-methyl-9H-2-purinyl)acetamide 
• 327161-45-5 N₁-[5-amino-4-chloro-6-(methylamino)-2-pyrimidinyl]acetamide 
• 232254-95-4 N₁-[4-chloro-6-(methylamino)-5-nitro-2-pyrimidinyl]acetamide 
• 74-87-3 methylene chloride 
• 74-83-9 methyl bromide 

Downstream Products

• 247193-36-8 6-chloro-2-iodo-9-methyl-9H-2-purine 
• 1175556-97-4 N-(6-chloro-9-methyl-9H-purin-2-yl)benzamide 
• 152833-01-7 O⁶-benzyl-9-methylguanine 
• 5502-78-3 7-methylguanine 
• 848648-62-4 C₁₃H₉ClN₆ 
• 327161-49-9 1-[2-(6-chloro-9-methyl-9H-2-purinyl)-1-ethynyl]-1-cyclohexanol 
• 920317-01-7 6-(dimethylamino)-9-methyl-9H-purin-2-amine 
• 61580-66-3 2-amino-6-methoxy-9-methyl-9H-purine 

Relevant academic research and scientific papers

Regioselective alkylation reaction of purines under microwave irradiation

The alkylation of purines which is generally carried out after anion formation by treatment with a base and alkyl halide is complicated and in the best cases, mixtures of N-alkylated compounds are obtained. Purine derivatives can be acquired from alkylati

The discovery of purine-based agents targeting triple-negative breast cancer and the αB-crystallin/VEGF protein–protein interaction

Oestrogen receptor-negative breast cancer, particularly subtypes such as triple-negative breast cancer (TNBC, around 10–15% of cases), are characterised by poor long-term survival, poor response to therapy and early progression to metastasis. Purine-based compounds represent a privileged scaffold in anticancer drug design, with several clinically approved and experimental agents in clinical development comprising a purine core structure. In this study, a series of new purine-based compounds were synthesised; seven of the new analogues were found to significantly reduce the in vitro viability of TNBC cell lines (MDA-MB-231 and MDA-MB-436) with IC50 values of ≤50 μM. In previous work, we have proposed a new concept for targeting angiogenesis driving TNBC progression, by disrupting the protein–protein interaction between the molecular chaperone αB-crystallin (CRYAB) and VEGF. Since previous clinical studies applying anti-VEGF therapy to TNBC patients have met with limited success, we were interested to test our most promising purine analogues against CRYAB/VEGF, using a custom-designed cell-based CRYAB/VEGF165 interaction assay platform. Analogues 4e and 4f significantly reduced the interaction between CRYAB/VEGF165, and compound 4e (100 μM) was also found to decrease the levels of soluble VEGF expressed by MDA-MB-231 cells by 40%. In conclusion, these promising early activity profiles warrant further investigation to validate this concept.

Tricyclic purine analogs derived from 2-amino-6-chloropurine and 2,6-diaminopurine and their methylated quaternary salts

A novel series of tricyclic, etheno-bridged purine analogs was sythesized from 2-amino-6-(substituted amino)-9-methylpurines by cyclization with chloroacetaldehyde, with particular focus on the regioselectivity of the cyclization reaction and fluorescence properties. The analogs as well as the starting purines were alkylated with iodomethane, affording a new class of quaternary salts with potential biological activity. Neither significant fluorescence nor cytostatic effect was found.

HIV REPLICATION INHIBITING PURINE DERIVATIVES

The present invention relates to the use of a compound of formula (I) for the manufacture of a medicament for the prevention or the treatment of HIV infection wherein the compound of formula (I) is a compound of formula (I) a N-oxide, a pharmaceutically a

6-Guanidinopurine nucleosides and their analogues

A general synthetic approach to 6-guanidinopurines, their ribonucleosides, 2-deoxyribonucleosides, acyclic nucleoside analogues and acyclic nucleoside phosphonates was developed. The approach consists in the reaction of the 6-chloropurine derivatives with guanidine solution in DMF under DABCO catalysis. This method was used to synthesize 6-guanidinopurine and 2-amino-6-guanidinopurine derivatives. Acyclic nucleosides and acyclic nucleoside phosphonates were also obtained by alkylation of the 6-guanidinopurine bases.

2-alkynyl-8-aryl-9-methyladenines as novel adenosine receptor antagonists: Their synthesis and structure-activity relationships toward hepatic glucose production induced via agonism of the A2B receptor

Novel adenosine antagonists, 2-alkynyl-8-aryl-9-methyladenine derivatives, were synthesized as candidate hypoglycemic agents. These analogues were evaluated for inhibitory activity on N-ethylcarboxamidoadenosine (NECA)-induced glucose production in primar

Identification of novel purine and pyrimidine cyclin-dependent kinase inhibitors with distinct molecular interactions and tumor cell growth inhibition profiles

Substituted guanines and pyrimidines were tested as inhibitors of cyclin B1/CDK1 and cyclin A3/CDK2 and soaked into crystals of monomeric CDK2. O6- Cyclohexylmethylguanine (NU2058) was a competitive inhibitor of CDK1 and CDK2 with respect to ATP (K(i) values: CDK1, 5 ± 1 μM; CDK2, 12 ± 3 μM) and formed a triplet of hydrogen bonds (i.e., NH-9 to Glu 81, N-3 to Leu 83, and 2-NH2 to Leu 83). The triplet of hydrogen bonding and CDK inhibition was reproduced by 2,6-diamino-4-cyclohexylmethyloxy-5-nitrosopyrimidine (NU6027, K(i) values: CDK1, 2.5 ± 0.4 μM; CDK2, 1.3 ± 0.2 μM). Against human tumor cells, NU2058 and NU6027 were growth inhibitory in vitro (mean GI50 values of 13 ± 7 μM and 10 ± 6 μM, respectively), with a pattern of sensitivity distinct from flavopiridol and olomoucine. These CDK inhibition and chemosensitivity data indicate that the distinct mode of binding of NU2058 and NU6027 has direct consequences for enzyme and cell growth inhibition.

Synthesis of heteromine C from guanine

Heteromine C previously isolated from a Taipei folk medicine plant, has been synthesised for the first time by selective methylation reactions starting from guanine. Thermal rearrangement to 1-methylherbipoline takes place when heteromine C is heated. It is shown that treatment of O6,9- dimethylguanine with methyl iodide gives the O6,7,9-trimethylguaninium iodide with complete selectivity, while similar reaction on O6,7- dimethylguanine results in methylation both in the 3- and 9-position.

Synthesis and in vitro evaluation of novel 2,6,9-trisubstituted purines acting as cyclin-dependent kinase inhibitors

Novel C-2, C-6, N-9 trisubstituted purines derived from the olomoucine/roscovitine lead structure were synthesized and evaluated for their ability to inhibit starfish oocyte CDK1/cyclin B, neuronal CDK5/p35 and erk1 kinases in purified extracts. Structure